| View Larger Image | Spontaneous homologous recombination is decreased in Rad51C-deficient hamster cells [An article from: DNA Repair] | Digitalby G.A. Drexler (Author), S. Rogge (Author), W. Beisker (Author), Eckardt-Schupp (Author)
| List Price: | $8.95 | | | Available: | Available for download now |
| | Binding: | Digital | | Publisher: | Elsevier | | Publication Date: | October 05, 2004 |
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Product Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: The Chinese hamster cell mutant, CL-V4B that is mutated in the Rad51 paralog gene, Rad51C (RAD51L2), has been described to exhibit increased sensitivity to DNA cross-linking agents, genomic instability, and an impaired Rad51 foci formation in response to DNA damage. To directly examine an effect of the Rad51C protein on homologous recombination (HR) in mammalian cells, we compared the frequencies and rates of spontaneous HR in CL-V4B cells and in parental wildtype V79B cells, using a recombination reporter plasmid in host cell reactivation assays. Our results demonstrate that HR is reduced but not abolished in the CL-V4B mutant. We thus, provide direct evidence for a role of mammalian Rad51C in HR processes. The reduced HR events described here help to explain the deficient phenotypes observed in Rad51C mutants and support an accessory role of Rad51C in Rad51-mediated recombination. |
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